Hematology Practice Questions

Q: What is the initial treatment recommended for a newly diagnosed patient with CML?

Imatinib mesylate therapy. **Explanation:** Chronic Myeloid Leukemia (CML) is characterized by the presence of the **Philadelphia chromosome (t[9;22])**, which creates the **BCR-ABL1 fusion gene**. This gene encodes a constitutively active tyrosine kinase protein that drives uncontrolled granulocyte proliferation. **Why Imatinib is the Correct Answer:** **Imatinib mesylate** is a selective **Tyrosine Kinase Inhibitor (TKI)** that binds to the ATP-binding site of the BCR-ABL protein, effectively "switching off" the oncogenic signal [1], [2]. It is the established **first-line standard of care** for newly diagnosed CML in the chronic phase due to its high rates of complete cytogenetic response and superior safety profile compared to older therapies [1]. **Analysis of Incorrect Options:** * **A. Allogenic Bone Marrow Transplantation:** While it is the only curative treatment, it is now reserved for patients who fail TKI therapy (resistance) or progress to Blast Crisis, due to high procedural morbidity [1]. * **C. TNF-α:** Tumor Necrosis Factor-alpha has no established role in the primary management of CML. * **D. IFN-α:** Interferon-alpha was the treatment of choice before the advent of TKIs. It is now rarely used except in specific scenarios like pregnancy, where TKIs are contraindicated due to teratogenicity [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Monitoring:** The gold standard for monitoring response is **Quantitative RT-PCR** for BCR-ABL1 transcripts (Molecular Response) [1]. * **Side Effects:** Common side effects of Imatinib include **periorbital edema**, muscle cramps, and skin rashes. * **Second-generation TKIs:** Dasatinib and Nilotinib are used if Imatinib resistance develops [1]. * **T315I Mutation:** This specific mutation confers resistance to most TKIs; **Ponatinib** is the drug of choice here.

Q: Which of the following are clinical features characteristic of anemia?

All of the above. Explanation: Anemia is defined as a reduction in the oxygen-carrying capacity of the blood due to a decrease in red blood cell mass or hemoglobin concentration. The clinical features of anemia arise from two main mechanisms: **tissue hypoxia** and **compensatory cardiovascular responses.** [2] * **Option A (Pallor):** This is the most classic sign of anemia. It occurs due to reduced hemoglobin concentration in the blood and compensatory vasoconstriction of peripheral vessels to shunt blood toward vital organs. [1] It is best assessed in the conjunctiva, mucous membranes, and palmar creases. [1] * **Option B (Increased heart rate):** To maintain oxygen delivery to tissues despite low hemoglobin, the body increases cardiac output. This is achieved primarily through an increase in heart rate (tachycardia) and stroke volume, reflecting a **hyperdynamic circulation.** [1] * **Option C (Mid-systolic flow murmur):** In anemia, blood viscosity decreases. This reduced viscosity, combined with increased flow velocity (hyperdynamic state), creates turbulence across the heart valves. This typically results in a soft, mid-systolic "flow" murmur, usually heard best at the pulmonary area. Since all three features are direct clinical manifestations of the body's adaptation to anemia, **Option D** is the correct answer. **High-Yield NEET-PG Pearls:** * **Hyperdynamic State:** Anemia is a common cause of high-output heart failure. * **Koilonychia:** Spoon-shaped nails are a specific sign of Iron Deficiency Anemia. [1] * **Pica:** Craving for non-nutritive substances (ice, dirt) is highly suggestive of iron deficiency. * **Angular Stomatitis/Glossitis:** Often seen in Vitamin B12, Folate, and Iron deficiencies. [1]

Q: Which of the following can cause Disseminated Intravascular Coagulation (DIC)?

All of the above. Disseminated Intravascular Coagulation (DIC) is a thrombo-hemorrhagic disorder characterized by the systemic activation of the coagulation cascade, leading to widespread fibrin deposition in the microvasculature and subsequent consumption of clotting factors and platelets [1]. **Why "All of the above" is correct:** DIC is always secondary to an underlying pathology that triggers the release of tissue factor (TF) or causes endothelial injury. * **Leukemia (Option A):** Specifically, **Acute Promyelocytic Leukemia (APL/M3)** is a classic cause. The malignant promyelocytes release procoagulant granules and tissue factor, triggering massive thrombin generation. * **Massive Transfusion (Option B):** Large-volume blood replacement can trigger DIC through several mechanisms, including the introduction of procoagulant phospholipids from stored blood, citrate toxicity, and underlying trauma/hemorrhagic shock which causes endothelial damage. [2] * **Abruptio Placentae (Option C):** Obstetric complications are a leading cause of DIC. In placental abruption, there is a massive release of **tissue thromboplastin** (tissue factor) from the placenta and decidua into the maternal circulation. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause overall:** Sepsis (Gram-negative organisms due to endotoxins). * **Laboratory Hallmarks:** Prolonged PT/aPTT, **decreased Fibrinogen** (best prognostic marker), thrombocytopenia, and **elevated D-dimer** (most sensitive). * **Peripheral Smear:** Presence of **Schistocytes** (fragmented RBCs) indicating microangiopathic hemolytic anemia (MAHA). * **Treatment:** Always treat the underlying cause first. Support with Platelets/FFP if bleeding occurs. In APL-induced DIC, **ATRA** (All-trans retinoic acid) is used.

Q: In hemophiliac patients, which of the following should not be given?

Platelet factor. ### Explanation **Correct Option: D (Platelet factor)** **Reasoning:** Hemophilia (A and B) is a disorder of **secondary hemostasis** caused by a deficiency in clotting factors (Factor VIII or IX) [1]. It is not a disorder of primary hemostasis (platelets). Platelet factor (or platelet transfusions) is indicated for thrombocytopenia or platelet dysfunction, neither of which is present in hemophilia. Giving platelet factor provides no therapeutic benefit to a patient lacking soluble clotting factors, making it the least appropriate choice. **Analysis of Incorrect Options:** * **A. Factor VIII concentrate:** This is the **treatment of choice** for Hemophilia A [1]. Recombinant or plasma-derived concentrates provide the specific missing factor required to stabilize the fibrin clot. * **B. Cryoprecipitate:** While less commonly used today due to the risk of transfusion-transmitted infections, cryoprecipitate contains Factor VIII, von Willebrand factor, and fibrinogen [1]. It remains a viable emergency option if specific concentrates are unavailable. * **C. EACA (Epsilon-Aminocaproic Acid):** This is an **antifibrinolytic agent**. It is frequently used as an adjunctive therapy in hemophilia, particularly for mucosal bleeds (like dental extractions), as it prevents the breakdown of the fragile clots that do manage to form [1]. **Clinical Pearls for NEET-PG:** * **Inheritance:** X-linked recessive (mostly affects males) [1]. * **Lab Findings:** Isolated **prolonged aPTT**; normal PT, normal bleeding time, and normal platelet count. * **Mixing Study:** The prolonged aPTT **corrects** when the patient's plasma is mixed with normal plasma (distinguishes deficiency from inhibitors). * **Desmopressin (dDAVP):** Useful in **Mild Hemophilia A** as it releases stored Factor VIII from Weibel-Palade bodies in endothelial cells [1]. It is ineffective in Hemophilia B.

Q: A 50-year-old male presents with massive splenomegaly. Which of the following conditions is NOT a likely cause of this presentation?

Aplastic anemia. **Explanation:** The hallmark of **Aplastic Anemia** is bone marrow failure leading to peripheral pancytopenia. Crucially, the bone marrow is "empty" (hypocellular), and there is no extramedullary hematopoiesis or infiltration by malignant cells. Therefore, **splenomegaly is characteristically absent** in aplastic anemia. If a patient with pancytopenia presents with an enlarged spleen, clinicians must look for alternative diagnoses like aleukemic leukemia or hypersplenism. **Analysis of Incorrect Options:** * **Chronic Myeloid Leukemia (CML):** This is the classic cause of **massive splenomegaly**. The spleen enlarges due to the sequestration of excess mature and maturing granulocytes [1]. * **Polycythemia Rubra Vera (PRV):** Splenomegaly occurs in approximately 75% of cases due to extramedullary hematopoiesis and congestion [1]. It can become massive if the disease progresses to the myelofibrotic phase. * **Hairy Cell Leukemia (HCL):** This is a B-cell lymphoproliferative disorder where the spleen is the primary site of disease. Massive splenomegaly is a defining clinical feature, often accompanied by "dry tap" on bone marrow aspiration. **NEET-PG High-Yield Pearls:** 1. **Massive Splenomegaly (Spleen >8cm below costal margin or >1kg):** Remember the mnemonic **"CHCC"** — **C**ML, **H**airy Cell Leukemia, **C**hronic Malaria (Tropical Splenomegaly Syndrome), and **C**ala-azar (Visceral Leishmaniasis). Myelofibrosis is another top cause [1]. 2. **Pancytopenia with Splenomegaly:** Think of Cirrhosis (portal HTN), Kala-azar, or Gaucher’s disease. 3. **Pancytopenia WITHOUT Splenomegaly:** Think of Aplastic Anemia, Vitamin B12/Folate deficiency, or PNH.

Q: Gaisbock's syndrome refers to:

Spurious erythrocytosis. **Gaisbock’s syndrome**, also known as **Spurious Erythrocytosis** or Stress Polycythemia, is a condition characterized by an elevated hematocrit and hemoglobin concentration despite a **normal total red cell mass**. The underlying pathophysiology is a **contraction of plasma volume**, which leads to hemoconcentration. It typically affects middle-aged, hypertensive, and often overweight individuals who may be under significant emotional or physical stress. **Analysis of Options:** * **A. Spurious erythrocytosis (Correct):** This is the defining feature of Gaisbock’s syndrome [1]. Unlike Polycythemia Vera (Primary) or Hypoxia-driven erythrocytosis (Secondary), there is no actual increase in the production of red blood cells; the "increase" is relative due to low plasma volume. * **B & C. Spurious/Reactive thrombocytosis (Incorrect):** These refer to elevated platelet counts. Spurious thrombocytosis can occur due to cell fragments (e.g., schistocytes) being miscounted as platelets, while reactive thrombocytosis is an elevated count due to inflammation or iron deficiency. Neither is associated with Gaisbock’s syndrome. * **D. Reactive erythrocytosis (Incorrect):** This is a form of secondary absolute polycythemia where red cell mass is truly increased, usually in response to high erythropoietin levels (e.g., chronic hypoxia or smoking). **High-Yield Clinical Pearls for NEET-PG:** * **Key Diagnostic Feature:** Normal Red Cell Mass + Decreased Plasma Volume [1]. * **Typical Profile:** "Stressed," hypertensive, obese male smokers [1]. * **Risk Factors:** Diuretic use (which further reduces plasma volume), tobacco use, and alcohol consumption [1]. * **Management:** Focuses on lifestyle modifications (weight loss, smoking cessation) and controlling hypertension rather than phlebotomy.

Q: Which of the following is NOT true about Multiple Myeloma?

Plasmacytosis < 10%. ### Explanation **1. Why Option D is the correct (False) statement:** The diagnosis of Multiple Myeloma (MM) requires the presence of **clonal bone marrow plasma cells ≥ 10%** [1] (or biopsy-proven extramedullary plasmacytoma) along with evidence of end-organ damage (CRAB features) or specific biomarkers of malignancy. A plasmacytosis of **< 10%** is characteristic of **MGUS** (Monoclonal Gammopathy of Undetermined Significance), not Multiple Myeloma. **2. Analysis of Incorrect Options:** * **A. Bence Jones protein in urine:** These are monoclonal free light chains (kappa or lambda) filtered by the glomerulus [1]. They are a classic finding in MM and can cause "Myeloma Kidney" (cast nephropathy). * **B. Hypogammaglobulinemia:** While there is a massive increase in one specific monoclonal antibody (M-spike), the production of normal, functional immunoglobulins is suppressed [1]. This leads to secondary hypogammaglobulinemia, making patients highly susceptible to encapsulated bacterial infections. * **C. Amyloidosis:** Approximately 10–15% of MM patients develop **AL (Light Chain) Amyloidosis**, where light chains deposit in tissues, leading to organ dysfunction (e.g., macroglossia, nephrotic syndrome, or restrictive cardiomyopathy). **3. High-Yield Clinical Pearls for NEET-PG:** * **CRAB Criteria:** **C**alcium (Hypercalcemia), **R**enal insufficiency, **A**nemia (Normocytic), **B**one lesions (Lytic "punched-out" lesions) [1]. * **Diagnosis:** Bone marrow biopsy is the gold standard. Look for "Flame cells" or "Mott cells." * **Investigation of Choice for Bone:** Whole-body low-dose CT or MRI (X-rays are traditional; Bone scans are usually negative because there is no osteoblastic activity). * **M-Spike:** Usually IgG (>50%) followed by IgA. * **Rouleaux Formation:** Seen on peripheral smear due to increased ESR/paraproteins [1].

Question 1

What is the initial treatment recommended for a newly diagnosed patient with CML?

Accepted Answer

Imatinib mesylate therapy

Answer

Allogenic bone marrow transplantation

Answer

TNF-a

Answer

IFN-a

Question 2

Which of the following are clinical features characteristic of anemia?

Accepted Answer

All of the above

Answer

Pallor of mucous membranes

Answer

Increased heart rate

Answer

Mid-systolic flow murmur

Question 3

Which of the following can cause Disseminated Intravascular Coagulation (DIC)?

Accepted Answer

All of the above

Answer

Leukemia

Answer

Massive transfusion

Answer

Abruptio placentae

Question 4

Megaloblastic anemia is seen in which of the following conditions?

Accepted Answer

Ileal resection

Answer

Crohn's disease

Answer

Intestinal lymphatic ectasia

Answer

Menetrier's disease

Question 5

Urgent reversal of warfarin therapy can be achieved by administration of which of the following?

Accepted Answer

Fresh frozen plasma

Answer

Cryoprecipitates

Answer

Vitamin K and fresh frozen plasma

Answer

Packed red cells

Question 6

In hemophiliac patients, which of the following should not be given?

Accepted Answer

Platelet factor

Answer

Factor VIII concentrate

Answer

Cryoprecipitate

Answer

EACA

Question 7

A 50-year-old male presents with massive splenomegaly. Which of the following conditions is NOT a likely cause of this presentation?

Accepted Answer

Aplastic anemia

Answer

Chronic myeloid leukemia

Answer

Polycythemia rubra vera

Answer

Hairy cell leukemia

Question 8

A 60-year-old woman complains of weakness and hematuria. Physical examination shows marked pallor, hepatosplenomegaly, and numerous ecchymoses of the upper and lower extremities. A CBC reveals a normocytic normochromic anemia, thrombocytopenia, neutropenia, and a marked leukocytosis, which is composed mainly of myeloblasts. The major clinical problems associated with this patient's condition are most directly related to which of the following?

Accepted Answer

Suppression of Hematopoiesis

Answer

Avascular necrosis of bone

Answer

Disseminated Intravascular Coagulation

Answer

Hypersplenism

Question 9

Gaisbock's syndrome refers to:

Accepted Answer

Spurious erythrocytosis

Answer

Spurious thrombocytosis

Answer

Reactive thrombocytosis

Answer

Reactive erythrocytosis

Question 10

Which of the following is NOT true about Multiple Myeloma?

Accepted Answer

Plasmacytosis < 10%

Answer

Bence Jones protein in urine

Answer

Hypogammaglobulinemia

Answer

Amyloidosis

Hematology — MCQs

Hematology — MCQs

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